Light induced photoreceptor degeneration occurs at surprisingly low light exposure in vivo in all species tested. The large concentration of unsaturated fatty acids in the rod outer segment (ROS) lipids and the known potency of light in inducing oxidative reactions leads to the hypothesis that photoreceptor degeneration is caused by lipid oxidation. This research first proposes to develop methods to eliminate lipid oxidation and other forms of structural degradation during extraction and purification of ROS membranes. Second, a functional assay for the ROS disk membrane will be sought. Third, lipid oxidation in purified ROS, outer segment free retinas and the pigment epithelium will be measured as a function of light exposure, dietary antioxidants (e.g. tocopherol and selenium) dietary proxidants (e.g. unsaturated fats) and animal age. These measurements will be correlated with photoreceptor degeneration as measured by ERG, electron microscopy and ROS disk membrane function (if a functional assay is found). If the hypothesis appears to be true the experiments will also give information on the natural protective mechanisms and will suggest means of dietary protection against photoreceptor degeneration. Furthermore, the function of primate macular pigment as a protective agent against photodynamic action will be investigated.